What is Fibromyalgia?

fibro - a Latin word meaning fibrous tissues, such as tendons and ligaments.

my - from the Greek word "myo" meaning muscles

algia - a Greek word meaning pain.

So fibromyalgia literally means "fibrous tissue and muscle pain." That name initially seemed appropriate since fibromyalgia was originally thought to be a musculoskeletal disorder because most of the pain was felt in the muscles and other soft tissues.

Much research and the advancement of brain-imaging technology, however, lead to the belief currently held by most that fibromyalgia is actually a disorder of the central nervous system, which causes abnormal pain processing and results in pain amplification. Longtime FM researcher, Dr. Daniel Clauw, describes fibromyalgia as "the poster child for a 'centralized' pain state."

While central sensitization certainly does seem to play a significant role in fibromyalgia, new research is revealing additional physiological factors which seem to play key roles in this illness we call fibromyalgia.

Pathophysiology of Fibromyalgia

Theories abound as to the cause of fibromyalgia. Years of research have uncovered numerous physiological abnormalities associated with FM. Many pieces of the fibromyalgia puzzle have been discovered but so far no one has been able to determine exactly how all of those puzzle pieces fit together. In the end, it may turn out that there are several "causes," any one of which can trigger the cascade of symptoms we know as fibromyalgia. Only time and continued research will tell.

Below are some of the categories of abnormalities found in fibromyalgia.

As technology improves and better brain-imaging techniques are developed, evidence that there are multiple brain abnormalities involved in fibromyalgia continues to grow. Following are just a few of the more recent studies confirming differences in the fibromyalgia brain.

Reduced Gray Matter Density: Fibromyalgia has been associated with alterations in brain morphometry (shape and size). In a 2009 study, researchers found a significant reduction in gray matter density within the bilateral parahippocampal gyri, right posterior cingulate cortex, and left anterior cingulate cortex - areas involved in functions related to the typical fibromyalgia symptoms, including enhanced pain perception, cognitive dysfunction, and abnormal stress reactivity.

Decreased Brain Connectivity: Findings from a 2014 study suggest "that abnormal connectivity patterns between pain-related regions and the remaining brain during rest reflect an impaired central mechanism of pain modulation in FM. Weaker coupling between pain regions and prefrontal- and sensorimotor areas might indicate a less efficient system level control of pain circuits."

Altered Central Processing: According to a 2014 study conducted at the University of Colorado Boulder, fibromyalgia patients reported increased unpleasantness in response to multi-sensory stimulation in daily life activities. Furthermore, fMRI displayed reduced activation of both the primary and secondary visual and auditory areas of the brain, and increased activation in sensory integration regions. These brain abnormalities mediated the increased unpleasantness to visual, auditory and tactile stimulation that patients reported to experience in daily life.

Pleasure/Pain Brain Signals Disrupted: A 2013 study indicates that a disruption of brain signals for reward and punishment contributes to increased pain sensitivity, known as hyperalgesia, in fibromyalgia patients. The results suggest that this altered brain processing might contribute to widespread pain and lack of response to opioid therapy in patients with fibromyalgia.

Abnormal Cerebral Blood Flow: In 2008, using single photon emission computed tomography (SPECT), researchers in France were able to detect functional abnormalities in certain regions in the brains of patients diagnosed with fibromyalgia, reinforcing the idea that symptoms of the disorder are related to a dysfunction in those parts of the brain where pain is processed. The researchers confirmed that patients with the syndrome exhibited brain perfusion abnormalities in comparison to the healthy subjects. Further, these abnormalities were found to be directly correlated with the severity of the disease. An increase in perfusion (hyperperfusion) was found in that region of the brain known to discriminate pain intensity, and a decrease (hypoperfusion) was found within those areas thought to be involved in emotional responses to pain.

A 2014 study also showed abnormal cerebral blood flow in fibromyalgia patients. This study demonstrated that the cognitive impairment in fibromyalgia was associated with alterations in cerebral blood flow responses during cognitive processing.

It has long been recognized that people with fibromyalgia often have other comorbid conditions - also referred to as overlapping conditions - like irritable bowel syndrome, migraine disease, restless leg syndrome, myofascial pain syndrome and multiple chemical sensitivity, to name just a few. In 1984, Dr. Muhammad Yunus used a Venn diagram to depict the overlap between these illnesses and put forth the idea that one thing they all had in common was central sensitization.

Several years later, Dr. Yunus suggested these conditions be unified under the term "central sensitivity syndromes." As with most new medical theories, physicians in general were hesitant to accept Dr. Yunus' idea. But eventually, they got on board and central sensitization is now the most widely accepted explanation of what is going on with fibromyalgia.

Central sensitization is defined by an exaggerated response of the central nervous system (CNS) to both stimuli that would be expected to be painful and stimuli that normally would not be considered painful, such as touch or massage. This exaggerated response can be triggered by a physical trauma, another chronic painful condition, or in some cases, by significant emotional stress. It is thought that in many cases of fibromyalgia, there is a genetic predisposition to the illness, which is then triggered by one of the events just mentioned.

In the May-August 2002 issue of Fibromyalgia AWARE magazine, Dr. Yunus describes what happens next when central sensitization is triggered. "As a result of the remarkable changes in the CNS following a stimulus, several things happen:

a normally painful stimulus becomes much more painful than expected (hyperalgesia);

a normally non-painful stimulus such as touch, gentle pressure or massage now becomes painful (allodynia);

What causes these changes following a painful stimulus? Several neurochemicals/neurotransmitters are involved, including substance P, neurokinin A, N-methyl-D-aspartate (NMDA), glutamate and aspartate. The fact that fibromyalgia patients typically show increased levels of substance P and decreased levels of the serotonin metabolite 5-hydroxyindole acetic acid in their cerebrospinal fluid further supports the idea of central sensitization.

In the same article, Dr. Yunus states, "The process of sensitization involves not only the intensity of pain, but also its quality (burning, tearing, pins and needles and other emotional reactions to pain). It also concerns the sustenance of pain (making it chronic and self-driven) and an expansion of the receptive field, making the pain widespread."

Small Fiber Neuropathy: One of the newest and most exciting areas of study related to fibromyalgia involves small nerve fibers. Several studies have found significantly reduced densities of small nerve fibers in approximately 30-40% of fibromyalgia patients. That in itself is a pretty large subset but some researchers think they've only scratched the surface. Thus far, testing has only been done on two parts of the body. They speculate that testing on other parts of the body (like perhaps the tender points) may reveal many more fibromyalgia patients who have small fiber neuropathy.

Cort Johnson has written a series of articles for his Health Rising blog that examine the small fiber neuropathy studies as they relate to fibromyalgia. If you would like to learn more about small fiber neuropathy and fibromyalgia, this is an excellent place to start:

Nerve Fibers in the Palms: Another study involving nerve fibers made the news in 2013. Only this time, instead of reduced densities of small nerve fibers, researchers found excessive sensory nerve fibers around specialized blood vessel structures located in the palms of the hands.

Dr. Frank Rice, president of the research company INTIDYN and senior researcher, explained how the excessive sensory nerve fibers could account for the widespread pain and fatigue that occurs in fibromyalgia.

"In addition to involvement in temperature regulation, an enormous proportion of our blood flow normally goes to our hands and feet. Far more than is needed for their metabolism. As such, the hands and the feet act as a reservoir from which blood flow can be diverted to other tissues of the body, such as muscles when we begin to exercise. Therefore, the pathology discovered among these shunts in the hands could be interfering with blood flow to the muscles throughout the body. This mismanaged blood flow could be the source of muscular pain and achiness, and the sense of fatigue which are thought to be due to a build-up of lactic acid and low levels of inflammation fibromyalgia patients. This, in turn, could contribute to the hyperactivity in the brain."

Dr. Phillip Albrecht, who also worked on the project, pointed out that alterations of normal blood flow may underlie other fibromyalgia symptoms, such as non-restful sleep or cognitive dysfunctions. "The data do appear to fit with other published evidence demonstrating blood flow alterations to higher brain centers and the cerebral cortex of fibromyalgia patients,"he stated.

Drs. Andrew Holman and Patrick Wood have led the way in research related to dopamine dysfunction in fibromyalgia.

Dopamine is a neurotransmitter in the brain that acts as a messenger so nerves can communicate with each other. According to Dr. Wood, "One of the important functions of brain dopamine is to serve as a natural pain killer - when a person experiences pain, the brain releases extra dopamine to fight the pain."

One of the first clues that there might be a connection between fibromyalgia and dopamine came from a 1992 study conducted by Dr. I. Jon Russell, et al., which showed lower than normal concentrations of metabolites of dopamine, norepinephrine, and serotonin in the cerebrospinal fluid of fibromyalgia patients.

A second hint that dopamine may play a role in fibromyalgia came from the fact that a lot of fibromyalgia patients also had restless legs syndrome (RLS), which was being successfully treated with drugs that stimulate the dopamine receptors.

Following is just a sampling of studies that support the dopamine/fibromyalgia hypothesis.

Of his 2007 study of dopamine activity in fibromyalgia, Dr. Wood said, "Our study demonstrated that female FM patients make significantly less brain dopamine than similarly aged women without the disorder. Not only does the brain make less dopamine, it does not release it properly when a patient experiences pain. Since dopamine serves in part to filter essentially all sensory input, a lack of dopamine results in a person experiencing non-painful stimulation (e.g. simple touch) as being painful."

In 2005, Dr. Holman conducted a clinical trial testing the effectiveness of pramipexole, an RLS drug and dopamine agonist. Forty-two percent of those taking the pramipexole achieved a 50% or greater decrease in pain. The pramipexole seemed to be most effective for a subset of fibromyalgia patients who required opioid analgesics and/or were disabled.

In a study published in 2009, Dr. Patrick Wood, et al. demonstrated a correlation between the reductions in gray matter density found in fibromyalgia and abnormal dopamine metabolism.

In a 2007 personal interview, Dr. Holman explained his theory about what may cause fibromyalgia and what role dopamine plays.

It all begins with the fight-or-flight response. The fight-or-flight response is a physiological reaction that occurs in response to a perceived harmful event. It's purpose is to protect us in times of danger by mobilizing a lot of energy very rapidly in order to cope with whatever is threatening us. Normally, the fight-or-flight response turns itself off once the perceived threat has passed. But sometimes it gets stuck in the "on" position. We then find ourselves living in a state of chronic stress.

What causes our fight-or-flight response to get stuck? Possibly a lack of dopamine. Dopamine is a neurotransmitter from a part of the brain called the hippocampus, whose job it is to control the brain stem activity that controls our fight-or-flight response.

When that happens, the fight-or-flight response begins to inhibit our sleep. We're no longer able to get into stage 4 sleep, which our bodies need to function properly and to regenerate our neurotransmitters. Dr. Harvey Moldovsky, who has done extensive research on sleep, has shown that it doesn't take long for people who are deprived of stage 4 sleep to develop many of the symptoms of fibromyalgia - pain amplification, fatigue, cognitive problems, etc.

Supporting Dr. Holman's theory is the PET scan data Dr. Wood gathered showing a lack of dopamine in the hippocampus of fibromyalgia patients. Additional support is the fact that pramipexole stimulates the dopamine 3 receptor, which he believes then restores the hippocampus function. Restoring the hippocampus allows it to control the brain stem, turn off the fight-or-flight response and restore stage 4 sleep. His clinical observation has been that fibromyalgia improves significantly and can, on occasion, disappear entirely.

It's important to remember that even if the dopamine hypothesis is correct, it will not apply to every person with fibromyalgia. There are other subsets of fibromyalgia with other causes.

Three types of cervical spinal cord compression have been implicated in some cases of fibromyalgia.

Positional Cervical Cord Compression: Positional Cervical Cord Compression (PC3) was first described by Dr. Daniel Heffez in 2002. He showed that the cervical canal - the long, bony tube that protects the spinal cord in the neck - can change shape with movement. For people with PC3, leaning their head back to look up can cause significant pain.

PC3 is diagnosed by doing a flexion-extension c-spine MRI. That's simply a regular MRI with two additional views. The regular MRI is done with your neck and head in the normal midline position. The additional views are one with your neck bent forward and another with your neck bent backward. The images of those with PC3 will show a narrowing of the cervical canal and compression of the cervical spinal cord when the neck is bent backward.

A study, conducted by Dr. Andrew Holman and published in The Journal of Pain in 2008, reported that 71% of the fibromyalgia patients he tested had PC3. In 2010, researchers from Oregon Health & Sciences University reported finding PC3 in 55% of fibromyalgia patients.

Unfortunately, it is difficult to find a radiologist who is willing to do the two additional views because they will only be paid for the one initial view. Currently, this three-view protocol is only routinely available in Milwaukee, Seattle and Portland.

Approximately 10% of PC3 cases require surgery but most can be effectively treated by a specialized physical therapy program and/or medication.

Chiari Malformation: Chiari malformations (CMs) are structural defects in the cerebellum, the part of the brain that controls balance. Normally the cerebellum and parts of the brain stem sit in an indented space at the lower rear of the skull, above the foramen magnum (a funnel-like opening to the spinal canal). When part of the cerebellum is located below the foramen magnum, it is called a Chiari malformation.

CMs may develop when the bony space is smaller than normal, causing the cerebellum and brain stem to be pushed downward into the foramen magnum and into the upper spinal canal. The resulting pressure on the cerebellum and brain stem may affect functions controlled by these areas and block the flow of cerebrospinal fluid to and from the brain.

Because a number of the symptoms of fibromyalgia and Chiari malformation are similar, it was once thought that CMs might be a possible cause of fibromyalgia. However, a 2011 study found that CMs were no more prevalent in the fibromyalgia community than they were in the general population.

Even if CM is not a cause of fibromyalgia, it is possible that what is actually a Chiari malformation could be misdiagnosed as fibromyalgia. It's also possible that a person could have both FM and CM. Therefore, if there is any question of a possible Chiari malformation, it's worthwhile to investigate further.

Cervical Spinal Stenosis: Cervical spinal stenosis, also called cervical myelopathy, is a narrowing of spaces in the cervical (neck) area of the spine that results in pressure on the spinal cord and/or nerve roots and possible obstruction of the flow of cerebrospinal fluid.

While some people inherit a small spinal canal, it is most often results from a gradual, degenerative aging process. Either structural changes or inflammation can begin the process. As people age, the ligaments of the spine may thicken and calcify (harden from deposits of calcium salts). Bones and joints may also enlarge.

As with PC3 and Chiari malformation, many of the symptoms of cervical spinal stenosis are very similar to those of fibromyalgia. In 2007, Dr. Dan Heffez, et al. Conducted a study comparing the outcome of surgical versus non-surgical treatment of cervical myelopathy in patients with fibromyalgia. They found that "There was a striking and statistically significant improvement in all symptoms attributed to the fibromyalgia syndrome in the surgical patients but not in the non-surgical patients at 1 year following the treatment of cervical myelopathy."

We can't be sure whether any or all of these types of cervical spinal cord compression are misdiagnosed as fibromyalgia, can trigger fibromyalgia, or occur along with fibromyalgia. What is important is that patients who have one of these forms of cervical spinal cord compression be properly diagnosed and treated. Eliminating the pain and other symptoms caused by cervical spinal cord compression should also improve many of the symptoms attributed to fibromyalgia.

History of Fibromyalgia

People often think of fibromyalgia as a relatively new illness because the term "fibromyalgia" wasn't used until late in the 20th century and it didn't have an official criteria until 1990. However, physicians and researchers have written about FM-like conditions since the early 1800s. And historical accounts of illnesses with remarkably similar symptoms can be found as far back as circa 1500 BC.

What may be the earliest description of a condition resembling fibromyalgia can be found in the Biblical account of Job's physical anguish. Job laments, "I, too, have been assigned months of futility, long and weary nights of misery. Lying in bed, I think, 'When will it be morning?' But the night drags on, and I toss till dawn... And now my life seeps away. Depression haunts my days. At night my bones are filled with pain, which gnaws at me relentlessly." (Job 7:3-4 and 30:16-17 - NLT)

In the 19th century, Florence Nightingale, an English army nurse and Red Cross pioneer, became ill as she worked on the front lines during the Crimean War (1854 - 1856). She never fully recovered and was bedridden much of the time, suffering with unrelenting pain and fatigue, until her death in 1910.

The collection of symptoms we know today as fibromyalgia, has been called by a variety of other names. Beginning in the 1600s, fibromyalgia-like symptoms were diagnosed as muscular rheumatism. Then in 1904, Sir William Gowers coined the term "fibrositis" to describe a condition which he believed was caused by inflammation within muscle fibers. When further research did not confirm Gowers' inflammation theory, Dr. Philip Hench renamed the condition fibromyalgia in 1976. Although new findings will not likely lead to another name change, it should be noted that very recent research seems to be indicating that Gowers may have been right all along, as several studies have shown there to be at least some degree of inflammation involved with FM.

The tender points, used to identify fibromyalgia and differentiate it from other pain conditions, were first described by Dr. Hugh Smythe in 1972. They were used in the 1981 Yunus study, which was the first controlled clinical study to use known fibromyalgia symptoms and tender points as validation. It was also Smythe who, in the training sessions for the 1990 American College of Rheumatology FM criteria study, taught the other investigators how to do a tender point examination.

Fibromyalgia Milestones

Following are some of the significant milestones in the history of fibromyalgia:

Year

Event

1600s

Symptoms resembling fibromyalgia were given the name muscular rheumatism.

1816

Dr. William Balfour, surgeon at the University of Edinburgh, was the first to fully describe what would later be known as fibromyalgia.

1824

Dr. Balfour described what would become known as tender points.

1904

Sir William Gowers coined the term fibrositis, which literally means "inflammation of fibers," to identify the pain experienced by patients formerly diagnosed with muscular rheumatism.

1972

Dr. Hugh Smythe laid the foundation for the modern definition of fibromyalgia when he described widespread pain and tender points.

1975

The first sleep electroencephalogram study, which identified the sleep disturbances that accompany fibromyalgia, was performed.

1976

Dr. William Balfour, surgeon at the University of Edinburgh, was the first to fully describe what would later be known as fibromyalgia.

1981

Dr. Muhammad Yunus was the first to officially use the term fibromyalgia as a synonym for fibrositis in a scientific publication.

1987

The American Medical Association recognized fibromyalgia as a real physical condition.

1990

The American College of Rheumatology developed diagnostic criteria for fibromyalgia to be used for research purposes. However, since there was no other diagnostic tool available, the criteria soon began to be used by clinicians as a tool to help them diagnose fibromyalgia in patients.

1990s

The concept of neurohormonal mechanisms with central sensitization was developed.

2007

Lyrica (pregabalin) became the first drug to receive FDA approval for the treatment of fibromyalgia.

2008

Cymbalta (duloxetine) was the second drug to receive FDA approval for the treatment of fibromyalgia.

2009

Savella (milnacipran) followed as the third drug to receive FDA approval for the treatment of fibromyalgia.

2010

The American College of Rheumatology proposed a new set of diagnostic criteria which takes into account other common fibromyalgia symptoms, such as fatigue, sleep disturbances, and cognitive problems, as well as pain.

2011

Modifications to the 2010 Fibromyalgia Diagnostic Criteria were proposed.

2012

The Social Security Administration published a ruling (SSR 12-2p) explaining how disability claims examiners and judges should evaluate whether fibromyalgia constitutes a "medically determinable impairment" (MDI). While this ruling does not automatically grant disability benefits to someone with fibromyalgia, it does recognize that fibromyalgia is a legitimate impairment. Beyond that, claimants must still prove that they are too disabled to work.

2013

The 2013 Alternative Criteria for diagnosing fibromyalgia was proposed.

Controversies About Fibromyalgia

Fibromyalgia has had more than its share of controversies on its journey to become accepted as a legitimate disease. Huge progress has been made over the last three to four decades, but there is still a little ways to go before everyone in the medical community fully accepts fibromyalgia as a real illness that deserves to be treated as such.

Until 1981 when Dr. Muhammad Yunus, et al. published the first controlled study of the clinical characteristics of fibromyalgia and the first data-based criteria for diagnosing it in Seminars in Arthritis and Rheumatism, the general attitude toward fibromyalgia was that it was considered to be essentially the same thing as psychogenic rheumatism. It was thought to be unworthy of research or investigation, as evidenced by the fact that very little related to fibromyalgia was published during the 1960s and 1970s.

Dr. Yunus' paper was a very important first step toward gaining credibility for fibromyalgia. Slightly less than a decade later, the American College of Rheumatology would publish the first official criteria for fibromyalgia so that researchers could be sure they were studying homogeneous groups of patients.

Although fibromyalgia was slowly gaining a foothold in the field of rheumatology, much of the medical community had still either not heard of fibromyalgia at all or they thought it was a psychosomatic problem, requiring referral to a psychiatrist.

By the end of the 1990s, the Internet was becoming more popular and fibromyalgia patients began to find one another. Prior to the availability of the Internet, even if a patient was lucky enough to find a doctor who knew how to diagnose fibromyalgia, it was unlikely that she knew anyone else with the same diagnosis. Fibromyalgia patients felt very alone and often thought they were the only ones who had to live with these odd and painful symptoms.

The Internet was quickly adopted by patients in general and by fibromyalgia patients in particular. First they banded together to form support groups. It was a huge relief for patients to find out they were not alone; that there were a lot of other people out there who were experiencing the same set of symptoms.

The need for advocacy groups soon became apparent. Patients needed help and the medical community seemed to be moving much too slowly. Soon several nonprofit advocacy organizations and research foundations were founded with the mission of raising awareness about fibromyalgia and encouraging more research.

While significant strides were being made, unfortunately there was still a large percentage of physicians who remained skeptical about fibromyalgia. It didn't help that Dr. Frederick Wolfe, lead author of the paper that established the 1990 ACR diagnostic criteria for fibromyalgia, reportedly changed his mind and became quite vocal in promoting his new theory that fibromyalgia is merely a byproduct of depression, stress and social anxiety. Needless to say, this was a disappointment for the fibromyalgia community. But there was a light shining on the horizon.

The year 2007 became a banner year for fibromyalgia. It was then that the U.S. Food and Drug Administration (FDA) approved Lyrica, the first-ever drug to be approved for the treatment of fibromyalgia. Even though Lyrica would only improve symptoms for about 30-40% of fibromyalgia patients, its approval made a very big difference for all FM patients for several reasons.

Fibromyalgia suddenly had legitimacy. After all, the FDA wouldn't approve a drug for an illness that didn't exist.

Physicians who previously didn't want to treat fibromyalgia patients because they felt they had nothing to offer them, now had a medication to offer.

Pfizer, the pharmaceutical company who developed Lyrica, did extensive television advertising for its new product. Within a few short months, most people had heard of fibromyalgia and had at least a vague idea of what it was.

The additional approvals of Cymbalta in 2008 and Savella in 2009 further bolstered the credibility of fibromyalgia in the eyes of the medical community, the government and the general public.

Today more medical professionals than ever are familiar with fibromyalgia. However, if you peruse fibromyalgia forums, you'll see that there are still far too many doctors who either don't believe it is real or consider it a "wastebasket" diagnosis - a diagnosis they give when they can't figure out what is wrong.

Why Doesn't My Doctor Know More About Fibromyalgia?

You may wonder why there is still any disbelief given all of the research that shows very distinctive physiological abnormalities in fibromyalgia. One big reason, according to Dr. Kent Holtorf in his article "Why Doesn't My Doctor Know This?" is because most doctors do not read medical journals. And even when they do learn of new research, they are resistant to anything new that they did not learn in medical school. That's not just his opinion; it's the conclusion of a number of studies and articles published in the aforementioned unread medical journals.

In defense of the doctors, their negligence in acquiring new scientific knowledge is not just a matter of apathy. They are so overloaded with patients and paperwork, there simply isn't enough time to keep up. Unfortunately, it is the patients who suffer. According to a National Institute of Health study, "The lag between the discovery of more effective forms of treatment and their incorporation into routine patient care averages 17 years."

What Can Patients Do?

Fibromyalgia patients must be proactive and take charge of their own healthcare. Find a doctor who is knowledgable about fibromyalgia; or at the very least, find a doctor who is open and willing to learn. Try to keep up with the latest fibromyalgia research. (ProHealth publishes all new FM research so check our Fibromyalgia Health Center regularly.) Take copies of significant research abstracts, or the entire journal article when possible, to your doctor. If your doctor is unwilling to even look at new research, it's probably time to find a new doctor.

Who is at Risk for Developing Fibromyalgia?

Adult women appear to be at greater risk for developing fibromyalgia than men or children, however, it can affect all ages and both sexes. Historically, 75 to 90 percent of people diagnosed with FM have been women, but new information may eventually change those figures.

Fibromyalgia experts are finding that men often have fewer than the traditional 11 tender points required for diagnosis, yet meet all the other diagnostic criteria for fibromyalgia. And what was once thought to be "growing pains" in children may turn out to be a previously unrecognized form of fibromyalgia. Although fibromyalgia will probably still occur most frequently in adult women, we may soon discover it affects significantly more men and children than once thought.

A significant risk factor is family history, as there is growing evidence of a genetic component in fibromyalgia. If someone in your family has fibromyalgia, you may be at greater risk of developing it yourself.

Since fibromyalgia is usually triggered by an injury, illness, other chronic pain condition or sometimes prolonged emotional stress, those events can increase a person's risk for developing fibromyalgia - particularly if the person has a family history of FM.

Will I Get Better?

Dr. Bruce Campbell, who has a self-help website for fibromyalgia and chronic fatigue syndrome, says of the prognosis for fibromyalgia,

"Fibromyalgia is neither progressive, nor fatal. Just as there is no cure for CFS, there is no treatment that cures fibromyalgia. But, as with CFS, some patients experience a spontaneous recovery and many experience notable improvement. In fact, improvement is probably the most common outcome for fibromyalgia, experienced by half to two thirds or so of patients.
"As with CFS, the course of fibromyalgia may vary. The location and severity of pain can change over time. Symptoms can be intermittent, fluctuating or persistent. Triggers of symptom intensification may include excessive activity, inactivity, stress, trauma, repetitive motion, poor sleep, strong emotions and weather changes."

Patients who experience the greatest improvement are generally proactive and adopt a multi-disciplined approach to treatment, which may include a combination of medication, alternative/complementary therapies, nutritional supplements, exercise, a healthy eating plan and lifestyle adaptations.